Evidence map›Paper›PMID 25203323›Full record

ArticleCancer cell2014

The splicing factor RBM4 controls apoptosis, proliferation, and migration to suppress tumor progression.

Yang Wang, Dan Chen, Haili Qian, Yihsuan S Tsai, Shujuan Shao, Quentin Liu, Daniel Dominguez, Zefeng Wang

Abstract read
In one paragraph

Article in Cancer cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers.

0numbers the graph read from it
0cells of the map it votes in
159citing papers in PubMed
6.7field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

159 citing papers in PubMed, 230 citations in OpenAlex.

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  15. CircRNAAutophagy · 2025
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99 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

Yang WangInstitute of Cancer Stem Cell, Second Affiliated Hospital, Cancer Center, Dalian Medical University, Dalian 116044, China; Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA. Electronic address: yangwang@dlmedu.edu.cn.
Dan ChenDepartment of Pathology, First Affiliated Hospital. Dalian Medical University, Dalian 116001, China.
Haili QianState Key Laboratory of Molecular Oncology, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100021, China.
Yihsuan S TsaiDepartment of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA.
Shujuan ShaoKey Laboratory of Proteomics of Liaoning Province, Dalian Medical University, Dalian 116044, China.
Quentin LiuInstitute of Cancer Stem Cell, Second Affiliated Hospital, Cancer Center, Dalian Medical University, Dalian 116044, China.
Daniel DominguezDepartment of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA.
Zefeng WangDepartment of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA. Electronic address: zefeng@med.unc.edu.
UNC Lineberger Comprehensive Cancer CenterSecond Affiliated Hospital of Dalian Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNDalian Medical University · CNFirst Affiliated Hospital of Dalian Medical University · CN

Funding

PREDOCTORAL TRAINING IN PHARMACOLOGICAL SCIST32GM007040 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI NICHOLAS, ROBERT A · 1985 to 2019
$6.0M
Modulation of VEGF-A alternative splicing as new anti-angiogenic therapeuticsR01CA158283 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WANG, ZEFENG · 2011 to 2015
$1.4M
NCI NIH HHS R01 CA158283NCI NIH HHS R01-CA158283NIGMS NIH HHS T32 GM007040
6 · The paper itself

Abstract

Splicing dysregulation is one of the molecular hallmarks of cancer. However, the underlying molecular mechanisms remain poorly defined. Here we report that the splicing factor RBM4 suppresses proliferation and migration of various cancer cells by specifically controlling cancer-related splicing. Particularly, RBM4 regulates Bcl-x splicing to induce apoptosis, and coexpression of Bcl-xL partially reverses the RBM4-mediated tumor suppression. Moreover, RBM4 antagonizes an oncogenic splicing factor, SRSF1, to inhibit mTOR activation. Strikingly, RBM4 expression is decreased dramatically in cancer patients, and the RBM4 level correlates positively with improved survival. In addition to providing mechanistic insights of cancer-related splicing dysregulation, this study establishes RBM4 as a tumor suppressor with therapeutic potential and clinical values as a prognostic factor.

Indexed as

ApoptosisCell MovementCell ProliferationAlternative SplicingAnimalsBase Sequencebcl-X ProteinCarcinoma, Non-Small-Cell LungCell Line, TumorDisease ProgressionEnzyme ActivationFemaleGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateLung Neoplasmsbcl-X ProteinMTOR protein, humanNuclear ProteinsRBM4 protein, humanRNA-Binding ProteinsSerine-Arginine Splicing FactorsTOR Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID25203323
PMCPMC4159621
OpenAlexW2094488327

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.